Accelerated senescence of bone marrow erythrocyte precursors in myelodysplastic syndrome.

BACKGROUND

Myelodysplastic syndromes (MDS) represent a heterogeneous group of clonal hematopoietic disorders characterized by ineffective haematopoiesis, refractory cytopenia, and an increased risk of progression to acute myeloid leukaemia. This study investigates the presence of cellular senescence in bone marrow (BM) CD235a erythrocyte precursors of MDS patients and explores its correlation with anaemia.

METHODS

We assessed senescence-related markers and cell cycle distribution in BM CD235a erythrocyte precursors of MDS patients. Correlation analyses were conducted between the relative mRNA expression of p16, a key senescence regulator, and peripheral blood parameters.

RESULTS

MDS patients exhibited heightened cellular senescence characterized by increased SA-β-gal positivity, elevated p16 and p21 expression, reduced CyclinD1 levels, and elevated IL-6. Cell cycle analysis revealed G0/G1 phase arrest. Correlation analysis established a negative association between p16 expression and reticulocyte count, RBC count, haemoglobin concentration, indicating a direct link between BM erythrocyte precursors senescence and anaemia severity.

CONCLUSION

MDS patients have accelerated senescence of bone marrow erythrocyte precursors, which is related to their anaemia. The observed correlation underscores the potential significance of senescence-targeted interventions in managing anaemia in MDS.Bone marrow CD235a⁺ erythroid precursors in MDS patients exhibit accelerated senescence, characterized by cell cycle arrest and increased inflammatory markers. p16INK4A expression negatively correlates with anaemia severity, suggesting senescence as a key contributor to MDS-related anaemia.